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目的：观察ａＦＧＦ与细胞膜上特异受体结合后引起的细胞内信号转导途径，探讨ａＦＧＦ导致细胞增殖的机理。方法：以不同浓度的ａＦＧＦ处理ＡＧＺＹ－８３Ａ细胞，利用［γ－３２Ｐ］ＡＴＰ掺入外源性底物的方法测定受体的酪氨酸蛋白激酶活性（ＴＰＫ）及蛋白激酶Ｃ（ＰＫＣ）活性；用Ｆｕｒａ－２／ＡＭ为荧光指示剂测定［Ｃａ２＋］ｉ。结果：随着ａＦＧＦ浓度增加，ＴＰＫ及ＰＫＣ活性随之升高。当ａＦＧＦ浓度为１．１２μｇ／ｍｌ时ａＦＧＦ处理组的ＴＰＫ是对照组的４倍；膜ＰＫＣ活性也是对照组的４倍，胞浆ＰＫＣ活性是对照组的１．７５倍。［Ｃａ２＋］ｉ是对照组的３倍。结论：该细胞株中ａＦＧＦ受体具有ＴＰＫ活性。ＴＰＫ激活后进一步促进蛋白质和酶磷酸化，而使ＰＫＣ活性及［Ｃａ２＋］ｉ升高，即ＰＫＣ和Ｃａ２＋是ＴＰＫ的下游信号分子，进一步促进ｃ－ｆｏｓ、ｊｕｎ基因表达增加，导致细胞增殖
OBJECTIVE: To observe the intracellular signal transduction pathways that aFGF binds to specific receptors on the cell membrane and to investigate the mechanism of aFGF-induced cell proliferation. METHODS: AGZY-83A cells were treated with different concentrations of aFGF and the receptor tyrosine kinase activity (TPK) and protein kinase C (PKC) activity were measured by incorporation of [γ-32P]ATP into exogenous substrates. ; Determination of [Ca2+]i using Fura-2/AM as a fluorescent indicator. Results: As the concentration of aFGF increased, the activity of TPK and PKC increased. When the aFGF concentration was 1.12 μg/ml, the TPK in the aFGF-treated group was 4 times higher than that in the control group; the membrane PKC activity was also 4 times higher than that of the control group, and the cytoplasmic PKC activity was 1.75 times that of the control group. [Ca2+]i is 3 times that of the control group. Conclusion: The aFGF receptor has TPK activity in this cell line. The activation of TPK further promotes the phosphorylation of proteins and enzymes, and increases PKC activity and [Ca2+]i, ie, PKC and Ca2+ are downstream signaling molecules of TPK, which further promotes the expression of c-fos and jun genes, leading to cell proliferation.